Abstract:

The classical paradigm of radiation biology is based on the notion that ionizing particle has to traverse a nucleus of a living cell in order to damage genetic material either directly or via production of short living free radicals. After DNA damage is introduced it can be either safely repaired and the cell can continue divisions unaltered; or it can result in a failure to repair and cells death; or finally, upon misrepair, the cell would be carrying genetic alteration that could result in cancer or developmental abnormality. Therefore modern risk estimations are based on the notion that nucleus is the true target of radiation effects and those are essentially stochastic with linear dependence on the dose.
During the last two decades or so, a different idea was developed based on the observation that irradiated cells can communicate radiation induced stress signals to their unaffected neighbors and themselves become reprogrammed to maintained abnormal radiation-induced phenotype across multiple cellular divisions. Even more astonishingly this phenotype maybe transmitted by irradiated germ cells to unexposed progeny. Here we suggest that these non-targeted effects are maintained by epigenetic mechanisms and examine epigenetic underpinnings of bystander and transgenerational effects in vivo.